Public Health Law and Ethics: A Reader / Edition 3

Public Health Law and Ethics: A Reader / Edition 3

ISBN-10:
0520294661
ISBN-13:
9780520294660
Pub. Date:
10/02/2018
Publisher:
University of California Press
ISBN-10:
0520294661
ISBN-13:
9780520294660
Pub. Date:
10/02/2018
Publisher:
University of California Press
Public Health Law and Ethics: A Reader / Edition 3

Public Health Law and Ethics: A Reader / Edition 3

$65.0 Current price is , Original price is $65.0. You
$63.68 
  • SHIP THIS ITEM
    Not Eligible for Free Shipping
  • PICK UP IN STORE
    Check Availability at Nearby Stores
  • SHIP THIS ITEM

    Temporarily Out of Stock Online

    Please check back later for updated availability.


Overview

Public Health Law and Ethics: A Reader, 3rd Edition probes the legal and ethical issues at the heart of public health through an incisive selection of judicial opinions, scholarly articles, and government reports. Crafted to be accessible to students while thorough enough for use by practitioners, policy makers, scholars, and teachers alike, the reader can be used as a stand-alone resource or alongside the internationally acclaimed Public Health Law: Power, Duty, Restraint, 3rd Edition. 

This updated edition reader includes new discussions of today’s most pressing health threats, such as chronic diseases, emerging infectious diseases, antimicrobial resistance, biosecurity, opioid overdose, gun violence, and health disparities.


Product Details

ISBN-13: 9780520294660
Publisher: University of California Press
Publication date: 10/02/2018
Edition description: Third Edition
Pages: 656
Sales rank: 746,923
Product dimensions: 5.90(w) x 8.90(h) x 1.60(d)

About the Author

Lawrence O. Gostin is University Professor and Founding  Linda D. and Timothy J. O’Neill Professor of Global Health Law at Georgetown University, where he directs the O'Neill Institute for National and Global Health Law. He is also the director of the World Health Organization Collaborating Center on National and Global Health Law and Professor of Public Health at Johns Hopkins University.
 
Lindsay F. Wiley is Professor of Law at American University’s Washington College of Law where she directs the Health Law and Policy Program. She is President of the American Society for Law, Medicine, and Ethics and a former member of the National Conference of Lawyers and Scientists.


Read an Excerpt

CHAPTER 1

Law and the Public's Health

Mapping the Terrain

The theory and practice of public health raise questions that are not resolved solely through scientific inquiry; rather, law and ethics guide the public health enterprise alongside epidemiology and biostatistics. Despite the close interplay among public health science, law, and ethics, each has its own methods and terminology. Until recently, cross-fertilization was rare. Most scholars and practitioners in the fields of law and ethics who have engaged in sustained examination of issues in health have focused principally on the financing and delivery of medical care and the conduct of medical research. The distinct perspectives and practices of public health have received far less attention. Fortunately, a growing number of practitioners, scholars, and organizations are developing public health law and public health ethics into fully fledged fields that stand alongside the related fields of health care law and bioethics.

Before applying ethics or law to problems in public health, it is important first to understand what we mean by public health. In this chapter, we highlight the prevention orientation, population perspective, and commitment to social justice that distinguish public health from medicine. We describe evolving models of public health science and practice, culminating in the social-ecological model. We conclude by surveying an ongoing debate over the legitimate scope of public health law, triggered by increased attention to noncommunicable diseases (e.g., cancer, heart disease, diabetes), injuries (e.g., motor vehicle, firearm, and overdose fatalities), and the social, economic, and environmental determinants of health in recent decades.

THE PREVENTION ORIENTATION AND THE POPULATION PERSPECTIVE

Public health inquiries and interventions are aimed at the prevention of injury, disease, and premature death at the population level. The Institute of Medicine (IOM) (1988, 19) in its landmark report The Future of Public Health proposed one of the most influential contemporary definitions of public health: "Public health is what we, as a society, do collectively to assure the conditions for people to be healthy." The IOM's emphasis on cooperative and mutually shared obligation ("we, as a society") reinforces that collective entities (e.g., governments and communities) take responsibility for healthy populations. The definition also adopts a broad focus on social, environmental, cultural, and economic factors ("the conditions for people to be healthy") that shape health-related behaviors and outcomes.

In the excerpt that follows, Rose offers a comparison between how medicine and public health approach questions of causation and methods for prevention. "Why did this patient get this disease at this time?" is a common question in medicine, underscoring a physician's principle concern for individuals. By contrast, those interested in public health seek knowledge about why ill health occurs in the population and how it can be prevented through structural, rather than individual, interventions.

SICK INDIVIDUALS AND SICK POPULATIONS

Geoffrey Rose

THE DETERMINANTS OF INDIVIDUAL CASES

In teaching epidemiology to medical students, I have often encouraged them to consider a question which I first heard enunciated by Roy Acheson: "Why did this patient get this disease at this time?" It is an excellent starting point, because students and doctors feel a natural concern for the problems of the individual. Indeed, the central ethos of medicine is seen as an acceptance of responsibility for sick individuals.

It is an integral part of good doctoring to ask not only, "What is the diagnosis, and what is the treatment?" but also, "Why did this happen, and could it have been prevented?" Such thinking shapes the approach to nearly all clinical and laboratory research into the causes and mechanisms of illness. Hypertension research, for example, is almost wholly preoccupied with the characteristics which distinguish individuals at the hypertensive and normotensive ends of the blood pressure distribution. Research into diabetes looks for genetic, nutritional and metabolic reasons to explain why some people get diabetes and others do not. The constant aim in such work is to answer Acheson's question, "Why did this patient get this disease at this time?"

The same concern has continued to shape the thinking of all of us who came to epidemiology from a background in clinical practice. The whole basis of the case-control method [(a retrospective study design in which researchers compare the history of individuals who have a condition ["cases"] to the history of individuals who do not ["controls"])] is to discover how sick and healthy individuals differ. Equally the basis of many cohort studies [(prospective studies in which researchers follow a group of similarly situated individuals over time to see which of them develops the condition of interest)] is the search for "risk factors," which identify certain individuals as being more susceptible to disease; and from this we proceed to test whether these risk factors are also causes, capable of explaining why some individuals get sick while others remain healthy, and applicable as a guide to prevention....

Unfortunately this approach to the search for causes, and the measuring of their potency, has to assume a heterogeneity of exposure within the study population. If everyone smoked 20 cigarettes a day, then clinical, case-control and cohort studies alike would lead us to conclude that lung cancer was a genetic disease; and in one sense that would be true, since if everyone is exposed to the necessary agent, then the distribution of cases is wholly determined by individual susceptibility. Within Scotland and other mountainous parts there is no discernible relation between local cardiovascular death rates and the softness of the public water supply. The reason is apparent if one extends the enquiry to the whole of the UK. In Scotland, everyone's water is soft [meaning that it contains low levels of calcium and magnesium]; and the possibly adverse effect becomes recognizable only when study is extended to other regions which have a much wider range of exposure. ... Even more clearly, a case-control study of this question within Scotland would have been futile. Everyone is exposed, and other factors operate to determine the varying risk. Epidemiology is often defined in terms of study of the determinants of the distribution of the disease; but we should not forget that the more widespread is a particular cause, the less it explains the distribution of cases. The hardest cause to identify is the one that is universally present, for then it has no influence on the distribution of disease.

THE DETERMINANTS OF POPULATION INCIDENCE RATE

I find it increasingly helpful to distinguish two kinds of etiological question. The first seeks the causes of cases, and the second seeks the causes of incidence. "Why do some individuals have hypertension?" is a quite different question from "Why do some populations have much hypertension, whilst in others it is rare?" The questions require different kinds of study, and they have different answers....

To find the determinants of prevalence and incidence rates, we need to study characteristics of populations, not characteristics of individuals. ... Within populations it has proved almost impossible to demonstrate any relation between an individual's diet and his serum cholesterol level; and the same applies to the relation of individual diet to blood pressure and to overweight. But at the level of populations it is a different story: it has proved easy to show strong associations between population mean values for saturated fat intake versus serum cholesterol level and coronary heart disease incidence, sodium intake versus blood pressure, or energy intake versus overweight. The determinants of incidence are not necessarily the same as the causes of cases....

PREVENTION

These two approaches to etiology — the individual and the population-based — have their counterparts in prevention. In the first, preventive strategy seeks to identify high-risk susceptible individuals and to offer them some individual protection. In contrast, the "population strategy" seeks to control the determinants of incidence in the population as a whole.

The "High-Risk" Strategy

This is the traditional and natural medical approach to prevention. If a doctor accepts that he is responsible for an individual who is sick today, then it is a short step to accept responsibility also for the individual who may well be sick tomorrow. Thus screening is used to detect certain individuals who hitherto thought they were well but who must now understand that they are in effect patients....

What the "high-risk" strategy seeks to achieve is something like a truncation of the risk distribution. This general concept applies to all special preventive action in high-risk individuals — in at-risk pregnancies, in small babies, or in any other particularly susceptible group. It is a strategy with some clear and important advantages....

The "high-risk" approach offers a more cost-effective use of limited resources. ... [I]t is more effective to concentrate limited medical services and time where the need — and therefore also the benefit — is likely to be greatest. ... If intervention must carry some adverse effects or costs, and if the risk and cost are much the same for everybody, then the ratio of the costs to the benefits will be more favorable where the benefits are larger.

Unfortunately the "high-risk" strategy of prevention also has some serious disadvantages and limitations. ... [I]t is palliative and temporary, not radical. It does not seek to alter the underlying causes of the disease but to identify individuals who are particularly susceptible to those causes. Presumably in every generation there will be such susceptibles; and if prevention and control efforts were confined to these high-risk individuals, then that approach would need to be sustained year after year and generation after generation. It does not deal with the root of the problem, but seeks to protect those who are vulnerable to it; and they will always be around.

The potential for this approach is limited — sometimes more than we could have expected — both for the individual and for the population. There are two reasons for this. The first is that our power to predict future disease is usually very weak. Most individuals with risk factors will remain well, at least for some years; contrariwise, unexpected illness may happen to someone who has just received an "all clear" report from a screening examination. One of the limitations of the relative risk statistic is that it gives no idea of the absolute level of danger....

This point came home to me only recently. I have long congratulated myself on my low levels of coronary risk factors, and I joked to my friends that if I were to die suddenly, I should be very surprised. I even speculated on what other disease — perhaps colon cancer — would be the commonest cause of death for a man in the lowest group of cardiovascular risk. The painful truth is that for such an individual in a Western population the commonest cause of death — by far — is coronary heart disease! Everyone, in fact, is a high-risk individual for this uniquely mass disease.

There is another, related reason why the predictive basis of the "high-risk" strategy of prevention is weak. It is well illustrated by ... the [correlation of] occurrence of Down's syndrome births to maternal age. Mothers under 30 years are individually at minimal risk; but because they are so numerous, they generate half the cases. High-risk individuals aged 40 and above generate only 13% of the cases. The lesson from this example is that a large number of people at a small risk may give rise to more cases of disease than the small number who are at a high risk. This situation seems to be common, and it limits the utility of the "high-risk" approach to prevention.

A further disadvantage of the "high-risk" strategy is that it is behaviorally inappropriate. Eating, smoking, exercise and all our other life-style characteristics are constrained by social norms. If we try to eat differently from our friends it will not only be inconvenient, but we risk being regarded as cranks or hypochondriacs. If a man's work environment encourages heavy drinking, then advice that he is damaging his liver is unlikely to have any effect. No one who has attempted any sort of health education effort in individuals needs to be told that it is difficult for such people to step out of line with their peers. This is what the "high-risk" preventive strategy requires them to do.

The Population Strategy

This is the attempt to control the determinants of incidence, to lower the mean level of risk factors, to shift the whole distribution of exposure in a favorable direction. In its traditional "public health" form it has involved mass environmental control methods; in its modern form it is attempting (less successfully) to alter some of society's norms of behavior.

The advantages are powerful. The first is that it is radical. It attempts to remove the underlying causes that make the disease common. It has a large potential — often larger than one would have expected — for the population as a whole....

The approach is behaviorally appropriate. If non-smoking eventually becomes "normal," then it will be much less necessary to keep on persuading individuals. Once a social norm of behavior has become accepted and (as in the case of diet) once the supply industries have adapted themselves to the new pattern, then the maintenance of that situation no longer requires effort from individuals. The health education phase aimed at changing individuals is, we hope, a temporary necessity, pending changes in the norms of what is socially acceptable.

Unfortunately the population strategy of prevention has also some weighty drawbacks. It offers only a small benefit to each individual, since most of them were going to be all right anyway, at least for many years. This leads to the Prevention Paradox (Rose 1981): "A preventive measure which brings much benefit to the population offers little to each participating individual." This has been the history of public health — of immunization, the wearing of seat belts and now the attempt to change various life-style characteristics. Of enormous potential importance to the population as a whole, these measures offer very little — particularly in the short term — to each individual; and thus there is poor motivation of the subject. We should not be surprised that health education tends to be relatively ineffective for individuals and in the short term. Mostly people act for substantial and immediate rewards, and the medical motivation for health education is inherently weak. Their health next year is not likely to be much better if they accept our advice or if they reject it. Much more powerful as motivators for health education are the social rewards of enhanced self-esteem and social approval....

CONCLUSIONS

The "high-risk" strategy of prevention is an interim expedient, needed in order to protect susceptible individuals, but only for so long as the underlying causes of incidence remain unknown or uncontrollable; if causes can be removed, susceptibility ceases to matter.

Realistically, many diseases will long continue to call for both approaches, and fortunately competition between them is usually unnecessary. Nevertheless, the priority of concern should always be the discovery and control of the causes of incidence.

* * *

Michael J. McGinnis and William H. Foege noted in 1993 that the biomedical model of record keeping and the societal need to explain a cause of death in terms of a discrete medical condition can distract the public from the root causes of disease. Medical explanations of death, often in the form of code numbers from the International Classification of Disease (ICD) on death certificates, point to discrete pathophysiological conditions or events, such as heart attack, stroke, cancer, diabetes, pneumonia, or suicide. In contrast, from the population perspective, McGinnis and Foege focused on what they labeled the "actual causes of death": tobacco, diet and activity patterns, alcohol, firearms, sexual behavior, motor vehicles, and illicit drug use. Ten years later, Ali H. Mokdad and his coauthors (2004) updated the statistics marshaled by McGinnis and Foege, noting trends in the leading modifiable causes of death over time. Sandro Galea and his coauthors (2011) built on this framework by assessing the impact of individual-level factors (e.g., educational attainment, household income, health insurance status, employment status, job stress, household conditions, level of social support, experience of racism or discrimination, housing conditions, and early childhood stressors) as well as community-level factors (e.g., area-level poverty, income inequality, deteriorating built environment, racial segregation, crime and violence, social capital, and availability of open or green spaces). They attributed approximately 245,000 premature deaths in the United States each year to low education, 176,000 to racial segregation, 162,000 to low social support, 133,000 to individual-level poverty, 119,000 to income inequality, and 39,000 to area-level poverty (Galea et al. 2011, 1462). Similarly, Anne Case and Angus Deaton (2017) have found that increases in "deaths of despair" (e.g., drug overdoses, suicides, and deaths due to alcohol-related liver disease) are attributable to a "long-standing process of cumulative disadvantage for those with less than a college degree," contributing to an overall increase in premature mortality among middle-aged non-Hispanic white people in recent years. Attributing deaths to economic despair, experiences of racism, early childhood stressors, and other social determinants of health may seem foreign to those accustomed to measuring mortality in terms of discrete medical causes such as cardiovascular disease or cancer. It is a powerful expression of the population perspective adopted by public health experts.

(Continues…)


Excerpted from "Public Health Law and Ethics"
by .
Copyright © 2018 The Regents of the University of California.
Excerpted by permission of UNIVERSITY OF CALIFORNIA PRESS.
All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
Excerpts are provided by Dial-A-Book Inc. solely for the personal use of visitors to this web site.

Table of Contents

PART ONE. CONCEPTUAL FOUNDATIONS OF PUBLIC HEALTH LAW AND ETHICS

1. Law and the Public’s Health: Mapping the Terrain
2. Public Health Ethics: Science, Values, and the Regulation of Risk

PART TWO. LEGAL FOUNDATIONS OF PUBLIC HEALTH

3. Public Health Powers and Duties
4. Public Health and the Protection of Individual Rights: Due Process, Equal Protection, and the First Amendment
5. Public Health Governance: Administrative Agencies and Local Governments

PART THREE. MODES OF LEGAL INTERVENTION

6. Direct Regulation for the Public’s Health and Safety
7. Tort Liability as Indirect Regulation
8. Taxation, Spending, and the Social Safety Net

PART FOUR. PUBLIC HEALTH LAW IN CONTEXT

9. Surveillance and Public Health Research: Privacy, Security, and Confidentiality of Personal Health Information
10. Infectious Disease Prevention and Control
11. Public Health Emergency Preparedness and Response
12. Noncommunicable Disease Prevention
13. Injury and Violence Prevention
14. Health Justice

About the Authors
Index
From the B&N Reads Blog

Customer Reviews